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PubMed · 392579

Stinging insect allergy.

H L Pence
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Abstract

One to two million Americans have a history of systemic allergic reactions to stinging insects and must live with the knowledge that future stings could be catastrophic. Recent advances have been made in diagnosis and treatment of this problem. Pure venoms have been recognized to be superior to the whole body extract as diagnostic and treatment antigens. Use of pure venoms for immunotherapy gives far better protection than whole body extract for the allergic patient and represents a major advance in the field of allergy. The imported fire ant is very different from the other common stinging insects in its venom components, the type of local reactions caused by its sting, and the fact that whole body extract from this insect seems to be as good an antigen for diagnosis and treatment as pure venom. Although important discoveries about insect allergy have been made recently, some very important questions are yet to be answered. Among these are: (1) Can suppliers of venom provide us with enough venom to treat all patients with insect allergy? (2) How long should immunotherapy be continued? and (3) Would treatment with specific antigens from venom be superior to using whole venom? We all await the answer to these and other questions with hopeful anticipation.

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AnaphylaxisAnimalsAntsBee VenomsHumansHymenopteraHypersensitivityImmunotherapyInsect Bites and StingsJournal ArticleReview

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H L Pence. 1979. Stinging insect allergy.. https://pubmed.ncbi.nlm.nih.gov/392579/

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Anaphylaxis↗
PubMed2003

Anaphylactic shock caused by immunoglobulin E sensitization after retreatment with the chimeric anti-interleukin-2 receptor monoclonal antibody basiliximab.

BACKGROUND: Repeated administration of chimeric or humanized monoclonal antibodies is generally well tolerated. Anti-idiotypic sensitization is rare and is considered to be of no clinical significance. We observed a child who experienced anaphylactic shock when he received a second course of basiliximab at the time of his second renal transplantation. We therefore searched for the presence of anti-basiliximab immunoglobulin (Ig) E in this patient. METHODS: Serum levels of anti-basiliximab IgE, assay of the anti-murine reactivity of circulating anti-basiliximab IgE, and assays for serum anti-mouse antibodies and global anti-basiliximab anti-idiotypic antibodies were carried out by enzyme-linked immunosorbent assay. Anti-basiliximab IgE antibodies on circulating basophils were evaluated by the ability of the patient's blood to produce leukotrienes in vitro after exposure to basiliximab. RESULTS: Sequential assays of serum samples by enzyme-linked immunosorbent assay indicated that anti-basiliximab IgE antibodies appeared after the second basiliximab course. There was no IgE reactivity toward a control murine IgG2a monoclonal antibody (mAb), indicating that the IgE response was directed exclusively against basiliximab idiotypes. There was no IgE reactivity against the humanized anti-interleukin-2 receptor mAb daclizumab, which was derived from a distinct parental murine mAb. Patient basophils harvested months after the anaphylactic shock produced leukotrienes in vitro on exposure to basiliximab. CONCLUSIONS: Patients exposed to chimeric antibodies may develop an anti-idiotypic IgE response that can trigger anaphylactic shock on further exposure. Specific anti-idiotypic IgE may be bound to basophils even in the absence of circulating IgE.

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